ArticleTranslational oncology2012
Control of Glycolytic Flux by AMP-Activated Protein Kinase in Tumor Cells Adapted to Low pH.
Article in Translational oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Neospora caninum hijacks host PFKFB3-driven glycolysis to facilitate intracellular propagation of parasites.Veterinary research · 2025Article
- The protective effect of Saudi Arabian bee honey against excessive weight gain and obesity-related parameters in rats fed a high-fat diet.Frontiers in nutrition · 2025Article
- Role of AMPK in Regulation of Oxaliplatin-Resistant Human Colorectal Cancer.Biomedicines · 2022Article
- Regulation and role of CAMKK2 in prostate cancer.Nature reviews. Urology · 2022Review
- Dual Stimuli-Responsive Dynamic Covalent Peptide Tags: Toward Sequence-Controlled Release in Tumor-like Microenvironments.Journal of the American Chemical Society · 2021Article
- Article
- Review
- Glioma stem cells and their roles within the hypoxic tumor microenvironment.Theranostics · 2021Review
- Glycometabolic rearrangements--aerobic glycolysis in pancreatic cancer: causes, characteristics and clinical applications.Journal of experimental & clinical cancer research : CR · 2020Review
- Coenzyme Q10 in association with metabolism-related AMPK/PFKFB3 and angiogenic VEGF/VEGFR2 genes in breast cancer patients.Molecular biology reports · 2020Article
- AIF knockdown induce apoptosis and mitochondrial dysfunction in cochlear spiral ganglion neurons in vitro.Molecular medicine reports · 2020Article
- Adaptation to chronic acidic extracellular pH elicits a sustained increase in lung cancer cell invasion and metastasis.Clinical & experimental metastasis · 2020Article
- Therapeutic Targeting of Cancer Stem Cells: Integrating and Exploiting the Acidic Niche.Frontiers in oncology · 2019Review
- 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3 spatially mediates autophagy through the AMPK signaling pathway.Oncotarget · 2017Article
- A role forJournal of molecular endocrinology · 2017Article
- A spatiotemporal hypothesis for the regulation, role, and targeting of AMPK in prostate cancer.Nature reviews. Urology · 2017Review
- ASIC1a mediates the drug resistance of human hepatocellular carcinoma via the CaLaboratory investigation; a journal of technical methods and pathology · 2017Article
- Dysregulated metabolism contributes to oncogenesis.Seminars in cancer biology · 2015Review
- Is 5´-AMP-Activated Protein Kinase Both Jekyll and Hyde in Bladder Cancer?International neurourology journal · 2015Review
- Glycolytic genes in cancer cells are more than glucose metabolic regulators.Journal of molecular medicine (Berlin, Germany) · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor cells grow in nutrient- and oxygen-deprived microenvironments and adapt to the suboptimal growth conditions by altering their metabolic pathways. This adaptation process commonly results in a tumor phenotype that displays a high rate of aerobic glycolysis and aggressive tumor characteristics. The glucose regulatory molecule, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), is a bifunctional enzyme that is central to glycolytic flux and is downstream of the metabolic stress sensor AMP-activated protein kinase (AMPK), which has been suggested to modulate glycolysis and possibly activate isoforms of PFKFB, specifically PFKFB3 expressed in tumor cells. Our results demonstrated that long-term low pH exposure induced AMPK activation, which resulted in the up-regulation of PFKFB3 and an increase in its serine residue phosphorylation. Pharmacologic activation of AMPK resulted in an increase in PFKFB3 as well as an increase in glucose consumption, whereas in contrast, inhibition of AMPK resulted in the down-regulation of PFKFB3 and decreased glycolysis. PFKFB3 overexpression in DB-1 tumor cells induced a high rate of glycolysis and inhibited oxygen consumption, confirming its role in controlling glycolytic flux. These results show that low pH is a physiological stress that can promote a glycolytic phenotype commonly associated with tumorigenesis. The implications are that the tumor microenviroment contributes to tumor growth and treatment resistance.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.